Programmed cell death pathways are known to exist in most if not all organisms on Earth, ranging from microbes to man. Proteins that effect this function, also known as apoptosis, have been identified in human, other mammals, plants, protozoa, fungi, and bacteria, among other forms of life. In humans, these proteins target the mitochondria, causing permeabilization, dissipation of the membrane potential, activation of intracellular signaling pathways, and ultimate death of the cell. Eukaryotic pathogens also contain mitochondria, and mitochondria are now widely accepted by evolutionary biologists to be decedents of specialized symbiotic bacteria in eukaryotic cells.
Given these close parallels between mitochondria and bacteria, it is contemplated that specific human, eukaryotic or prokaryotic proteins have necessarily evolved to control prokaryotic symbionts (eg. mitochondria, chloroplasts) or competitors, and directly or indirectly prompt death of microbes or infected or abnormal cells. These types of proteins exhibit similarities in structures (eg., cationic helical domains) and mechanisms of action (eg., membrane interaction or perturbation that can lead to programmed cell death). Thus, such proteins may serve as excellent templates for novel therapeutic molecules, and reveal new insights into host-pathogen co-evolution, cancer biology, and other disease prevention, pathogenesis and treatment.